We study how vertebrate immune systems detect microbial molecules and how these microbial recognition systems evolve at the level of receptors, ligands, and gene regulation. A central focus is recognition of microbial proteins such as flagellin, a structural component of bacterial flagella that serves as a conserved microbial signal in host–microbe interactions.
We use Toll-like receptor 5 (TLR5) as a model system for microbial protein sensing, with particular emphasis on the diversification of TLR5 paralogs in centrarchid fishes (TLR5s and TLR5m). This system provides a natural framework for studying how microbial ligand recognition is maintained, modified, and functionally constrained across vertebrate evolution.
Using comparative genomics and phylogenetic analysis, we investigate how microbial sensing receptors evolve under selection imposed by microbial ligands such as flagellin, and how these evolutionary dynamics shape receptor function and signaling potential in innate immune pathways.
We analyze immune transcriptomic variation in inflammatory diseases including Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA) to study how microbial sensing and innate immune signaling pathways are reorganized across heterogeneous immune states.
We focus on how variation in host–microbe interaction programs, including responsiveness to microbial ligands and downstream innate immune signaling, maps onto differences in immune activation states across patient subsets. This includes pathway-level shifts in microbial sensing networks that reflect altered immune regulation in chronic inflammatory conditions.